Mechanisms of hypocalcaemia in the clinical form of severe magnesium deficit in the human

Abstract

Severe magnesium depletion leading to hypocalcaemia has been described in a variety of clinical settings. Inadequately low concentrations of parathyroid hormone (PTH) are a constant feature of hypomagnesaemic hypocalcaemia (HMHC), while target organ resistance to PHT in kidneys and bone may be demonstrated in the majority of these patients. The failure of membrane-bound adenylate cyclase in the parathyroids, kidneys and bone, thought to be the most important molecular mechanism in HMHC, cannot explain the concomitant resistance to vitamin D and its metabolites. In recent years, information has accumulated on further magnesium-dependent intracellular events and alternative pathways of transcellular signalling. This may eventually allow the identification of one or more further biochemical mechanisms leading to hypocalcaemia in severe magnesium deficiency.